pharm Flashcards
histamine triple response
red - vasodilation
wheal - increase permeabilty
flare - spreading response through sensory neurons
how does histamine cause acid secretion
acts on H2 R on parietal cell, to increase cAMP
activates K/H pum p
biosynthesis of bradykinin
prekallikrein converted to kallikrein by factor XII
kallikrein converts HMW kinninogen to bradykinin
C1 esterases
kallikreins
hereditary angioedema
deficiency in CI esterase inhibitor - use B2 R ant
activation and effects of NO
ach/bradykinin/sheer stress - causes increase Ca
Ca activates nitric oxide synthase
converts arginine to NO
NO activates guanylate cyclase to increase cGMP and cause relaxation
what regulates vascular tone
basal release of NO
symp or parasymp has greater influence on HR at rest
parasymp
symp action on heart
act on B1, increase cAMP, opens Ca channels - decrease time to reach potential, increase rate of firing, increase conduction time
3 mechanisms underlying dysrhythmias
- altered pulse formation - abnormal AP generation
- altered pulse conduction - conduction block, re-entry
- triggered activity - early or late afterdepolarisations:
- early - abberant Na or Ca channel opening
- late - Ca overload - excitation on completion of repolarisation
4 Classes of antidysrhythmics
- Na channel blockers - 1a, b,c
- B blockers
- K channel blockers
- Ca channel blockers
class 1 a b c antidysrhythmics
Na channel blockers
1a - quinidine - moderate block, prolong repolarisation, increase ERP
1b - lignocaine - mild block, shorten repolarisation, decrease ERP
1c - flecainide - big block, same repolarisation, same ERP
amiodarone
K channel blocker, also other ones
antihypertensives
a - angiotensin system inhibitors - Ace inhibitors, AngiR ants
b - B antagonists
c - L-type Ca blockers
d - diuretics
olols
B blockers
sartans
angI R ant
prils
ACE inhibitors
digoxin mehcanism of action
inhibits Na/K atpase, increase Na intracellular, decreases Ca extrusion - builds up in SR, increase Ca release with each AP
dobutamine
B agonist
heparin
enhances antithrombin 3 activity - inactivates factor Xa and thrombin
monitoring of heparin with
APTT
warfarin
inhibits vit K reductase - inhibits reduction of vit K, therefore inhibits gamma carboxylation in blood coagulation factors
monitor warfarin with
PT and INR
3 drugs affecting platelet activation/adhesion
ADP R ant
aspirin
GPIIb/IIIa R ant
fibrinolytic drugs
streptokinase
alteplase - hrtPA - clot selective, not antigenic
loop diuretics mech of action
block Na/K/Cl carrier in thick ascending limb
thiazide diuretics mech
inhibit Na/Cl in distal tubule
side effects of thiazide
K loss, increase uric acid
loop diuretics side effect
K loss, H loss - metabolic alkalosis
K Sparing diuretics mech
spironolactone - ald R ant - block Na channels and decreased Na/K pump synthesis
amiloride - Na luminal channel blocker
3 drugs that can damage kidney
mercury - toxicity and vasoconstriction
gentamicin - alters Ca metabolism
cisplatin - forms ROs
statins mech
HMG-CoA reductase inhibitors - decrease cholesterole synth so increase LDL R on liver and increase LDL uptake and increase HDL
bile acid sequestrants
prevent absorption cholesterol, increase excretion, increase demand for chol for bile acid syntheiss, increase LDL R adn removal of LDL
Ezetimibe
inhibits sterol transporter in intestine - only as adjacent to statin
treatment for hypertriglyceridaemia
fibrates - increase LPL so decrease TAGs in plasma
nicotinic acid
hypercholesterolaemia treatment - all statin things plus decreases atherogenic lipoprotein a - but poor tolerance
4 treatments for stable angina
- nitrates - No release
- Ca channel blockers - decrease afterload, HR, SV
- B blockers
- ivabradine
unstable angina treatment
as for stable plus aspirin
process of mast cell degranulation
FcR clustering - tyrosine K activity - PLC - Dag (PKC) and IP3 (Ca mobilisation) - degranulation
where cys-LT released from
eosins, masts, macs
cys-LT physiological role or path
only path
endogenous mast cell inhibitors
PGE2, Adrenaline, cortisol
disodium chromoglycate
causes annexin-1 releaes - inhibits cys-LT production
omalizumab
binds IgE
montelukast
cys-LT R ant for aspirin or exercise induced asthma
asthma airway hyperresponsiveness
airways constrict too easily and too much
SABA mech of action
B2 ag - Gs - PKA - activates SERCA, blocks Ip3 - both decrease Ca intracellular - decrease contraction
treatment of bronchoconstriction in COPD
anti-musc
actions of glucocorticoids in asthma
- decrease activity, recruitment, survival of eosins and Th2
- decrease mast cell activation and cytokine production
- decrease prolif, cyt and collagen production of smooth muscle adn fibroblasts
indication for inhaled GCS
if B2 ag needed more than 3 times a week
cell infiltration in COPD
neuts, CD8, lots of macs
Triple wammy
ace inhibitor - dilate efferent arteriole
diuretic - decrease volume
NSAID - vasoconstrict afferent arteriole
methotrexate
blocks human dihydrofolate reductase - anticancer, immunosuppressant
amphotericin
stops ergosterol synthesis - antifungal
paclitaxel
bind polymerised tubulin - prevents dissassembly therefore mitosis - anti cancer
short term infusion useful for what drugs
low TI
problem with low bioavailability
patient variability will have higher consequences
problem with slowly distributing drug
peak conc will be higher than expected based on Vd as in beginning its distributing in smaller compartment as hasnt reached fat or muscle yet
newborns deficinet in what metabolism enzymes
phase II
elderly deficient in what metabolism enzymes
phase I - CYT
what is pharmacokinetic drug drug interaction
drug a effects conc of drug b at receptor
what is pharmacodynamic drug drug interaction
drug a effects actions of drug b without altering conc at R
esomeprazole
PPI - H/K atpase - PUD
ranitadine
H2R ant - PUD
sodium bicarb
antacids
hyoscine butylbromide
musc R ant - smasmolytic
misoprostol
PGE2 anaolgue
promethazine
H1R ant - antiemetic - motion sick
hyoscine hydrobromide
M R ant - anti-emetic
metoclopramide
D2R ant (also blocks 5HT3 and 4 )- anti-emetic
prochlorperazine
D2R ant - less sedative - anti-emetic, extrapyramidal side effects
ondansetron
5HT3 R ant - antiemetic - no extrapyramidal side effects
aprepitant
NK1R ant - anti-emetic
4 laxatives
bulking agents
faecal softeners and lubricants - docusate
magnesium sulphate - osmotic laxative
senna - stimulant
antidiarrhoeals
loperamide - opioid
mebeverine - anti-spasmolytic
hyoscine butylbromide - anti-spasmolytic
treatment for gas
simethicone - defoaming agent
activated charcol
carminatives - peppermint, dil
two types of dose dependent side effects
on target and off target
what problem with terfenadine and grapefruit
terfenadine usually 0% bioavailable and converted to active metabolite
grapefruit competitively binds to CYP3A4 - terf becomes bioavailable and inhibits K channels - fatal ventricular arrhythmias
2 metabolism pathways of paracetamol
- conjugated to suphate or glucoronide metabolite
2. oxidised by CYP450 into intermediate metabolite and glutathione conjugates into non-toxic product
why does paracetamol toxicity occur
glutathione overwhelmed, ROS produced
epiphyses fusing in upper limb
cats make rob laugh capitulum - 1 med epicondyle - 5 radial head - 5 lat epicondyle, trochlea, olecranon- 10